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Effect of ODAM and BMPRIB on Enamel Mineralization
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¹ÚÁ¾Å ( Park Jong-Tae ) - ¿¬¼¼´ëÇб³ Ä¡°ú´ëÇÐ ±¸°»ý¹°Çб³½Ç
Á¶±¤Èñ ( Cho Kwang-Hee ) - Á¶¼±´ëÇб³ Ä¡°ú´ëÇÐ ±¸°ÇغÎÇб³½Ç
¹èÇö¼÷ ( Bae Hyun-Sook ) - ³²¼¿ï´ëÇб³ Ä¡À§»ýÇаú
Á¶¿µ½Ä ( Cho Young-Sik ) - ³²¼¿ï´ëÇб³ Ä¡À§»ýÇаú
±èÈïÁß ( Kim Heung-Joong ) - Á¶¼±´ëÇб³ Ä¡°ú´ëÇÐ ±¸°ÇغÎÇб³½Ç
KMID : 1023420110110010055
Abstract
The purpose of this study was to investigate the biological function of ODAM and its signal transduction pathway in the steps of ameloblast differentiation and enamel mineralization. An ODAM recombinant protein was produced and stable ODAM transgenic cell lines were also established using ameloblast-lineage cells (ALCs). To verify the ODAM signal transduction pathway, BAMBI recombinant protein, an inhibitor of BMP2 and BMP receptor 1B (BMPR-1B), was treated and BMPR-1B siRNA was used to silence expression of BMPR-1B. Mineralization was augmented by the ALCs treated with the ODAM recombinant protein and the sense ODAM overexpressing cells. The ALP activity was also increased markedly in the sense ODAM overexpressing cells and the ALCs treated with ODAM recombinant protein. The inactivation of ODAM in the ALCs down-regulated the expression of BMPR-1B, whereas its expression was up-regulated markedly when ODAM was overexpressed. These results provide deeper insights into the process of ameloblast maturation and in enamel mineralization. It also suggested that ODAM augmented enamel mineralization.
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Ameloblast; Enamel; Mineralization; Odontogenic ameloblast-associated protein (ODAM); Signal transduction system
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